Hepatitis C and the leptin system - Bound leptin levels are elevated in patients with hepatitis C and decrease during antiviral therapy

Background: Serum leptin levels are elevated in alcoholic liver cirrhosis a nd thus might be involved in the anorexia and hypermetabolism often seen in those patients. We hypothesized that the leptin system is modulated in pat ients with hepatitis C and might be affected by antiviral therapy. The aim of this study was to investigate the different leptin components in serum o f patients with hepatitis C before, during and after interferon alpha and r ibavirin therapy and in controls. Methods: 25 patients (11 female, 14 male) with chronic hepatitis C were compared with body mass index, gender and ag e-matched controls (n = 25). Patients were treated with interferon alpha al one (3 MU tiw) or in combination with ribavirin for 6-12 months. Free lepti n and bound leptin levels were measured using specific radioimmunoassays be fore interferon therapy, at 12 weeks of therapy and after 3 months of follo w-up. Results: Free leptin levels were higher in female than in male subjec ts, both for patients (P < 0.01) and controls (P < 0.05). Bound leptin leve ls were elevated in both female (P < 0.05) and male (P < 0.001) patients co mpared to controls. No alteration of free leptin levels was found during th erapy, whereas bound leptin levels decreased after 3 months of therapy (P < 0.005) and re-increased to the baseline levels 3 months after therapy was stopped. Responder but not non-responder had decreased bound leptin levels (P < 0.01) comparing pre- and posttreatment levels. However, no significant correlations were determined between any of the leptin components to virus load, ALT, TNF alpha receptor levels (sTNFR-75, sTNFR-55) and histopatholo gy at any time point. Conclusion: Since no correlation was found between th e different leptin components and any of the inflammatory markers, the decr ease in bound leptin levels during antiviral therapy suggests either a dire ct interferon-dependent effect on the leptin system or an alteration of oth er leptin secretagogues.